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Intramural haematoma of the thoracic aorta: who's to be alerted the cardiologist or the cardiac surgeon?
© Baikoussis et al; licensee BioMed Central Ltd. 2009
Received: 11 May 2009
Accepted: 1 October 2009
Published: 1 October 2009
This review article is written so as to present the pathophysiology, the symptomatology and the ways of diagnosis and treatment of a rather rare aortic disease called Intra-Mural Haematoma (IMH). Intramural haematoma is a quite uncommon but potentially lethal aortic disease that can strike as a primary occurrence in hypertensive and atherosclerotic patients to whom there is spontaneous bleeding from vasa vasorum into the aortic wall (media) or less frequently, as the evolution of a penetrating atherosclerotic ulcer (PAU). IMH displays a typical of dissection progress, and could be considered as a precursor of classic aortic dissection. IMH enfeebles the aortic wall and may progress to either outward rupture of the aorta or inward disruption of the intima layer, which ultimately results in aortic dissection. Chest and back acute penetrating pain is the most commonly noticed symptom at patients with IMH. Apart from a transesophageal echocardiography (TEE), a tomographic imaging such as a chest computed tomography (CT), a magnetic resonance (MRI) and most lately a multy detector computed tomography (MDCT) can ensure a quick and accurate diagnosis of IMH. Similar to type A and B aortic dissection, surgery is indicated at patients with type-A IMH, as well as at patients with a persistent and/or recurrent pain. For any other patient (with type-B IMH without an incessant pain and/or without complications), medical treatment is suggested, as applied in the case of aortic dissection. The outcome of IMH in ascending aorta (type A) appears favourable after immediate (emergent or urgent) surgical intervention, but according to international bibliography patients with IMH of the descending aorta (type B) show similar mortality rates to those being subjected to conservative medical or surgical treatment. Endovascular surgery and stent-graft placement is currently indicated in type B IMH.
Intramural haematoma (IMH) belongs to "acute aortic syndrome" followed by penetrating atherosclerotic ulcer (PAU) and the classical acute aortic dissection. It occurs as a bleeding into the aortic wall (media) without initial rupture of the intima and the classic flap formation. Despite IMH of the thoracic aorta being a disease of the aorta, its optimal initial treatment still remains a hot debatable issue. Aortic intramural haematoma can firstly appear to hypertensive and atherosclerotic patients who suffer an impulsive haemorrhage from vasa vasorum rupture into the media either spontaneously, or less commonly, as a result of PAU. Rarely does a thoracic trauma lead to IMH [1, 2]. According to records , the IMH can successfully be cured; lead to aortic dissection or in aortic rupture. The initial haematoma of the aortic wall may be augmented and further affect the medial layer of the aorta , similarly to the aortic dissection. Consequently, IMH weakens the aorta and may progress to either outward rupture of the aortic wall or inward disruption of the intima, which leads to aortic dissection [4–6]. Similarly to aortic dissection, IMH is divided in proximal (type A) and distal, without the ascending aorta being involved (type B). According to recommendations of the Task Force on aortic dissection, European Society of Cardiology, there are two types of IMH: Type I shows a smooth inner aortic lumen, the diameter usually being less than 3.5 cm, and the wall thickness is bigger than 0.5 cm [3, 7]. The Type II IMH occurs in aortic atherosclerosis. A rough inner aortic surface with severe aortic sclerosis is frequently noticed. The aorta is dilated to more than 3.5 cm and calcification is usually found. Mean wall thickness is 1.3 cm ranging from 0.6 to 4 cm [3, 7]. As far as the clinical impact of intramural haematoma is concerned, it has been documented that the cases of type A haematomas tend to have a high frequency of complications (dissection or rupture) even death, and therefore should be surgically treated in emergent or urgent setting [4, 8]. Contrary to the above, type B-distal, (descending aorta), IMH uncommonly progress to complications and is frequently completely resolved without any intervention . In the era of endovascular surgery the stent-graft placement in the descending aorta has an indication.
Pathogenesis and pathophysiology of the IMH
The common risk factors for cardiovascular diseases are to be held responsible in the pathogenesis of the IMH. Special circumstances, such as pregnancy as well as some congenital disorders should be taken into account. Arterial hypertension is the most frequent predisposing factor for IMH, present in 84% of the patient cohort and similarly to the 67% incidence, reported in a post mortem study of 161 cases of dissection [1, 9]. Nevertheless, as in the case of aortic dissection, the initiating event of acute IMH remains unknown. Nutrient vases called Vasa vasorum are present in most arteries, including the aorta and coronary arteries, carotids, and femoral arteries . Pathological neovascularization of the vessel wall is a consistent feature in the formation of atherosclerotic plaque and development of the disease [11, 12]. Additionally, microvessels are increased in coronary lesions from patients with acute myocardial infarction, suggesting a potential role of microvessels in plaque rupture and instability . Furthermore, microvessels play a role in plaque haemorrhage associated with the development of symptoms in cerebrovascular disease according to some reports [14, 15]. Gore  suggested that spontaneous rupture of aortic vasa vasorum may initiate aortic wall disintegration, eventually leading to dissection. Moreover, rupture of the nutrient vasa vasorum of the media layer may cause haematoma without a tear [3, 14]. Other authors have proposed intimal "fracture" of an atherosclerotic plaque as the primary event, which then allows propagation of blood into the aortic media causing intramural haematoma. Moreover, discrete penetrating atheromatous ulcers have also been thought as a prerequisite for intramural bleeding . In such a chronic setting, however, the haematoma is confined to the area nearest to the atherosclerotic ulcer. Although some uncertainty exists concerning how to distinguish IMH from limited aortic dissection with a thrombosed false lumen, IMH pathology has been identified as the very early stages of dissection with an impending risk of rupture [18, 19]. What is more, patients with intramural haematoma are also typically older than those with classic dissection, supporting the opinion that degenerative changes in the media play a key role in the IMH formation . There are some both acquired and genetic conditions leading to the breakdown in the integrity of the intima, which weaken the media layers of the aorta, and lead to a higher aortic wall stress [6, 20]. As a final result, these factors may induce an aortic dilation, aneurysm formation, intramural beeding, acute or chronic aortic dissection, or aortic rupture. Furthermore, the extracellular matrix may be subjected to degradation, apoptosis, and elastolysis, frequently at the limits of the atherosclerotic plaques [1, 2, 21]. However, a series of congenital abnormalities such as Marfan's syndrome, Ehlers-Danlos syndrome  annuloaortic ectasia, bicuspid aortic valve, and familial aortic dissection are the prime suspects, predisposing acute aortic syndromes [3, 7, 22]. Stefanadis's study carried out with dogs experimented, revealed that aortic wall distensibility decreased significantly to those with removed vasa vasorum of the aortic wall . Atherosclerosis leads to the thickening of the intima layer of the vases. Thickness of the intima increases the distance between the endothelial layer and the media, compromising the nutrient and oxygen supply while adventitial fibrosis may obstruct small intramural vasa vasorum. Reduced nutritional supply of the media results in media thinning following a necrosis due to the necrosis of the smooth muscle cells.  Advanced imaging technology (MDCT) has defined precursors or "variants" to frank aortic dissection such as IMH, PAU, and localized intimal tears [3–8, 23, 24]. Ramona Scotland et al characterize endothelin-1 (ET-1)-mediated contraction of vasa vasorum and investigate whether threshold concentrations of ET-1 alter any sensitivity to constrictors . Circulating plasma levels of ET-1 are elevated in several disease including atherosclerosis, hypertension, congestive heart failure asthma and diabetes. In our opinion, after the atheroschlerotic plaque destabilization, a spontaneous plaque rupture follows. As we know, vassels (vasa vasorum), are also present in the atheroschlerotic plaque matrix. Is it the plaque rupture that provokes immediately vasa vasorum rupture and intramural haematoma? The presence of several layers of smooth muscle implies that the vessels of the vasa vasorum actively regulate their own tone rather than serving as a passive channel for the blood flow. Many studies have been conducted with dogs in vivo supporting this hypothesis investigating vasa vasorum reactivity to vasoactive agents. Heistad suggested that the diameter of the vasa vasorum of canine thoracic aorta increases in response to intravenous infusion of adenosine .
Natural history and predictors for progress and complications of IMH.
There is some controversy concerning the natural history of acute IMH. It is known that IMH may either progress or regress in an extend way. [4, 23, 38, 39]. It originates from ruptured vasa vasorum in medial wall layers and results in an aortic wall infarct that may bring about a secondary tear, causing finally in some cases, a classic aortic dissection [23, 24]. IMH should be affronted with attention; in fact, aortic IMH is considered as a precursor or a possible cause of a later dissection [6, 6, 20]. Whereas IMH resorption has been reported in only 10% of cases, never has resorption of aortic dissection been reported [7, 8, 40, 41]. Studies of Kaji S et al and Neri E et al in 1999 and then Kaji S et al again in 2002 have suggested that IMHs reflect a more benign condition in which aggressive medical therapy and serial imaging may allow watchful waiting and the avoidance of surgery in some patients [42–44]. In IRAD study which registered 1010 patients with acute aortic dissection, 58 (5.7%) of them had IMH . They showed an association between increasing hospital mortality and the proximity of IMH to the aortic valve, regardless of any medical or surgical treatment [2, 27]. According to the international bibliography, [8, 45, 46], the IMH evolves to 1) resumption, 2) progression to classic aortic dissection, or 3) formation of an aneurysm within 30 days of hospital admission. A rate of 9 out of 12 deaths with IMH occurred in the ascending aorta, has been reported [2, 27]. The presence of IMH in the ascending aorta is commonly considered as an independent factor of progression to aortic aneurysm formation, aortic rupture and/or dissection [45, 46]. However, type A or proximal IMH is no longer related to early death when surgical intervention is performed [8, 45, 46]. According to Neinaber et al , a closer look reveals that 75% of proximal IMH patients died or had surgical replacement by the time of follow up. Alternatively, IMH of the descending aorta (type B or distal), may be treated conservatively or through endovascular intervention as elective cases [8, 24, 46, 47]. According to a study  on morbidity and mortality for 168 patients with IMH, in 25% of ascending aortic IMH and in 13% of descending IMH led to aortic dissection, in 28% and 9% to aortic rupture, in 28% and 76% to stabilisation, respectively. In this study the 30-day mortality was 18% with surgical repair of proximal IMH, and 33% with surgery to distal IMH compared to 60% and 8% with medical treatment of type A and type B IMH, respectively . Considering a 12% early mortality after surgery, and a 24% death rate with medical treatment, global experience from the International Registry of Aortic Dissection determined a tendency for a better outcome after surgery of proximal IMH [8, 46, 47]. It seems that IMH is similar to aortic dissection or better, to chronic aortic dissection. According to another study, the high risk of "wait and see" in type A IMH, is 55% early mortality with conservative - medical treatment compared to 8% with surgical repair . However, in 10 out of 22 patients (45%) with type A IMH underwent surgical repair and four cases after medical management developed cardiac tamponade . In another report  tamponade was observed in two out of three patients with type A IMH surviving medical treatment. According to records,, age and the use of β-blockers constitute factors of determining the progression of the IMH. In a report, only 7% of IMH with late progression were treated with β-blockers compared to 49% of IMH patients without late progression patients . In a study, predictor of late progression of IMH is the younger age (<49 years) , and medication without β-blockers [8, 45]. However, analysis of IMH confirmed better long term outcome in patients treated with β-blockers . β-blockers protect by reducing aortic wall stress and the systolic arterial blood pressure [28, 50]. Several controversies are present in this issue. There are not fixed predictor factors for early or late progression of IMH. Large series are necessaries in this setting. The observation that older age (> 55 years) at initial diagnosis of IMH has a better long term prognosis may be explained by more focal microscars along the aortic wall inherently limiting the longitudinal progression of IMH [8, 20, 22]. In reality, the IMH is considered  a class 2 aortic dissection.
Medical or surgical management of IMH?
IMH is a rare but potentially lethal disease of the aorta. Nevertheless, pathogenesis and risk factors should be examined, in detail. Clinical manifestations, diagnosis, and management of acute aortic syndrome should be codified for rapid and accurate treatment. IMH of the aorta is a potentially lethal disorder with frequent conclusion to aortic rupture, dissection or aneurysm. Short term prognosis is extremely serious in IMH involving the ascending aorta, and surgical repair improves the outcome. IMH of the descending aorta, especially when confined to a short segment or without dilatation has a better outcome. Endovascular treatment is an alternative way of treatment in individual cases with acceptable results. Long term prognosis, may be more beneficial from chronic effective β blockers regardless of surgical repair.
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